Abstract [en]

Respiratory dysfunction is common after major burns. The pathogenesis is, however, still under debate. The aim was to classify and examine underlying reasons for respiratory dysfunction after major burns. Consecutive adult patients (n = 16) with a total burned body surface area of 20% or more who required mechanical ventilation were assessed for acute respiratory distress syndrome (ARDS), inhalation injury, sepsis, ventilator-associated pneumonia (VAP), ventilator-induced lung injury (VILI), using conventional criteria, together with measurements of cardiovascular variables and viscoelastic properties of the lung including extravascular lung water.

Nine patients developed ARDS within 6 days of injury. ARDS was characterized by a large reduction in the PEEP-adjusted PaO2:FiO2 ratio, pulmonary compliance, and increased extra vascular lung water together with increased renal dysfunction rates. Seven patients fulfilled the criteria for inhalation injury. They also had decreased PaO2:FiO2 ratios. There was an increase in extra vascular lung water and a decrease in compliance measures though not to the same extent as in the ARDS group. White blood cell counts dropped from (mean) 21.4 x 10exp9 /l (95% CI 15.3-27.5) in day 1 to 4.3 x 10exp9 /l (2.2-6.5) on day 3, and lower values tended to correlate with the development of ARDS. Sepsis occurred before onset of ARDS in only three cases. One patient fulfilled the criteria for VAP, but none was thought to have VILI.

We found that respiratory dysfunction after burns is multifactorial, and ARDS and inhalation injury are most important. The early onset of ARDS, together with the changes in white blood cell count and organ dysfunction, favours a syndrome in which respiratory distress is induced by an inflammatory process mediated by the effect of the burn rather than being secondary to sepsis. The power of these conclusions is, however, hampered by the small number of patients in this study.

Abstract [en]

The number of patients who are admitted for in-hospital care in Sweden because of burns is about 12/100,000, and only a small proportion of these have larger burns. Among them, and particularly among those who die in hospital, a condition referred to as “organ dysfunction” is common and an important factor in morbidity and mortality. The fact that the time of the initial event is known, and the magnitude of the insult is quantifiable, makes the burned patient ideal to be studied. In this doctoral thesis organ dysfunction and mortality were studied in a descriptive, prospective, exploratory study (no interventions or control groups) in patients admitted consecutively to a national burn centre in Sweden.

The respiratory dysfunction that is seen after burns was found to be equally often the result of acute respiratory distress syndrome and inhalation injury. We found little support for the idea that this early dysfunction is caused by pneumonia, ventilator-induced lung injury, or sepsis. Acute kidney injury (AKI) was also common, and mortality was associated with severity. Importantly, renal dysfunction recovered among the patients who survived. Pulmonary dysfunction and systemic inflammatory response syndrome developed before the onset of AKI. Sepsis was a possible aggravating factor for AKI in 48% of 31 patients; but we could find no support for the idea that late AKI was mainly associated with sepsis. We found that older age (over 60 years), greater TBSA%, and respiratory dysfunction were associated with increased mortality, but there was no association between the overall mortality and sex. We also found that early transient liver dysfunction was common, and recorded early hepatic “hyper”- function among many young adults. Persistent low values indicating severe liver dysfunction were found among patients who eventually died.

We conclude from this investigation that overall organ dysfunction is an early and common phenomenon among patients with severe burns. Our data suggest that the prognosis of organ dysfunction among these patients is good, and function recovers among most survivors. Multiple organ failure was, however, the main cause of death. The findings of the early onset in respiratory dysfunction and a delay in signs of sepsis are congruous with the gutlymphatic hypothesis for the development of organ dysfunction, and the idea of the lung as an inflammatory engine for its progression. We think that the early onset favours a syndrome in which organ dysfunction is induced by an inflammatory process mediated by the effect of the burn rather than being secondary to sepsis.

Our data further suggest that clinical strategies to improve burn care further should be focused on early interventions, interesting examples of which include: selective decontamination of the gastrointestinal tract to prevent translocation of gut-derived toxic and inflammatory factors; optimisation of fluid replacement during the first 8 hours after injury by goal-directed resuscitation; and possible improvement in the fluid treatment given before admission.